The objective of this investigation is to study, mainly on the ultrastructural level, the formation of coloboma. The congenital defect is experimentally produced by teratogenic induction in two ways: (1) A single high dose of vitamin A is given to pregnant female golden hamsters after a certain time of gestation. (2) Young female hammsters are raised on a vitamin A deficient diet and bred at the age of three to four months. The females of both groups are sacrificed at various stages of pregnancy, between day 10 and 12 of gestation; the embryos are removed and their eyes processed for electron microscopy. Those eyes in which the embryonic fissure does not close due to the effect of vitamin A excess or vitamin A deficiency are studied by light and electron microscopy and examined for cells or subcellular structures which are involved in or responsible for the formation of the defect. By studying progressively younger developmental stages it is attempted to determine the age or stage at which the development of colobomatous eyes begins to deviate from that of normal eyes. In addition, the two types of induced coloboma are compared as to involvement of structures and onset of deviation from the normal development.